Browsing Tag: Hank

Honey. You’ve met honey. It’s that sticky,
sweet stuff. Basically just slightly liquidy sugar in a
plastic bear bottle, right? Wrong! Honey is a supercharged bacteria-killing
powerhouse. And it’s all down to what those hardworking bees put into it, from immune
proteins to the sugar itself. Since ancient times, honey has been used to
prevent wounds from getting infected. And these days, we use purified and standardized
versions of honey to fight infections in hospitals. Honey has three main tricks for fighting bacteria. The first is all that sugar. Honey is only about 17% water. Most–but not
all–of what remains is sugar. The two main types of sugar in honey are glucose
and fructose. Like all sugars, glucose and fructose are sticky — they attract water. Honey is technically a supersaturated solution,
meaning it contains more sugar than would normally dissolve at that temperature. That’s
why it eventually gets all crystally in the pantry — over time, the sugar comes out of
the solution. Chemically speaking, it’s desperate for
water. Water can travel across cell membranes from
where there’s a higher concentration of water to where there’s a lower concentration.
And there’s a higher concentration of water in a bacterium than in honey. Which means that honey will suck the juices
right out of any bacterium — or mold, or fungus — that tries to set up shop. Plus, there’s isn’t enough water in honey
for any microorganisms to live on. So they die, and the honey doesn’t spoil. The second thing, is that when bees make honey,
they throw in an enzyme called glucose oxidase. And bacteria hate glucose oxidase because
it produces two different compounds. It converts glucose to gluconic acid and hydrogen
peroxide. Gluconic acid is, you guessed it, an acid.
It gives honey a pH value of less than 4. That’s about a thousand times more acidic
than the neutral pH of 7 that most bacteria need to grow. And hydrogen peroxide is very good at killing
cells. It destroys the cell walls of bacteria, which breaks them apart. Glucose oxidase isn’t active in ripe honey–there’s
not enough water for it to work properly. It seems to be there to keep the honey from
spoiling while the bees are drying it out. But if you dilute honey, the glucose oxidase
will switch back on and make gluconic acid again. The final thing bees do to make honey antibacterial?
They put antibiotics in it. Some types of honey contain a protein called
bee defensin-1, which is exactly what it sounds like. Bee defensin-1 defends bees. It’s part of
their immune system and protects them from certain bacteria, including ones that could
cause nasty diseases inside the hive. It’s produced in a gland that bees use to
make honey, so it makes sense that some of it would make it into the finished product.
And while scientists aren’t sure how much of the protein is really in honey, it sort
of makes sense that bees would use it to protect their food. Another antibacterial compound sometimes found
in honey is methylglyoxal. Methylglyoxal is a small organic molecule
that forms in honey from a compound in the nectar of certain flowers. There’s an especially large amount of methylglyoxal
in manuka honey, a honey made from a New Zealand flower. This honey is so good at killing bacteria
that it’s actually used in hospitals. There’s one bacterium that has honey’s
number–but only sort of. It’s the type of bacteria that that causes
botulism. The bacteria start out as spores, which are
very hard to kill. They’re already dried out, so honey’s
water-sucking properties don’t kill them, and because the spores aren’t growing, they
aren’t affected by the acidity or the antibiotic compounds. The really dangerous part of the bacteria
is the botulinum toxin they produce when they grow into mature bacteria. Less than a hundred
nanograms — that’s billionths of a gram — is enough to kill an adult. About 10% of honeys have some botulinum spores
in them. But since the spores in honey aren’t growing and making toxin, they’re harmless
to healthy adults. Our immune systems intercept the spores before they can start growing inside
of us. But the immune systems of infants aren’t
always able to kill those spores before they start growing. So, in rare cases, the bacteria
can germinate and start producing toxin. That’s why it’s not safe to give honey
to infants under one year old, but the rest of us don’t need to worry about it. So the next time you’re looking for something
sweet, go ahead — eat some of bacteria’s worst enemy. Thanks for watching this episode of SciShow,
which was brought to you by our patrons on Patreon. Thank you, so much, to all of those
people. If you want to be one of those people you can go to patreon.com/scishow. And if
you just want to keep getting smarter with us, don’t forget to go to youtube.com/scishow
and subscribe!

{♫Intro♫} If you’re coughing, sneezing, or starting
to feel under the weather, you might blame a virus, or possibly a bacterium. Which is not something humans have known to
do for very long. Around 400 B.C.E., doctors might have blamed
an imbalance of the four vital humors for your illness. Around the 1700s, they might have pointed
to an invisible, disease-carrying fog instead. Today, we know pathogens — viruses, bacteria,
and certain other microbes — are responsible for many diseases. But linking specific diseases to the microbes
that cause them has been surprisingly tricky. In 1882, a scientist named Robert Koch demonstrated
that the bacterium Mycobacterium tuberculosis causes tuberculosis. And in 1890, he also published a framework
for future scientists to make similar discoveries. He created a checklist for researchers to
reference any time they’re trying to link a pathogen to a disease. The steps are as follows. First, researchers had to be able to find
the pathogen in sick organisms, but not healthy ones. Second, it could be grown in pure culture
— which means that a sample of the microbe could be taken from a sick organism, and then
the microbe could grow independently in a 19th century version of the petri dish. Third, if they exposed a healthy organism
to the stuff that they grew in step two, that organism would get sick with the same disease. Finally, though this step is sometimes considered
optional, the same microbe that was isolated in step one must be found again in the organism
made sick in step three. These steps are now known as Koch’s Postulates. The idea is that if the microbe meets all
of the postulates, then you know it’s the cause of the disease. Unfortunately, his postulates had a few problems. Take postulate one. Tuberculosis can actually be found in healthy
individuals — that’s called latent tuberculosis — so it doesn’t meet Koch’s first postulate. This situation just didn’t show up in his
experiments, which were done in guinea pigs. Postulate three isn’t perfect either. Assuming that any healthy organism exposed
to a pathogen will get sick ignores differences in immune systems. A healthy organism might be able to fight
off the infection or might already be immune to the disease. But it was the second postulate that caused
the most confusion. Something grown in “pure culture” has
to be the only living thing in the dish, and many pathogens just can’t grow independently
like that. Viruses, for example, reproduce by hijacking
molecular machinery in the cells of the organism they’re infecting. Meaning you can’t grow them in a dish by
themselves. But bacteria often grow in a dish just fine. Because postulate two required the thing to
grow in culture, researchers at the turn of the twentieth century would almost exclusively
blame bacteria for the diseases they were studying, which resulted in some false accusations. Malaria, which is actually caused by blood-infecting
parasites, was blamed on a bacterium from Italian marshes in the 1880s, which they named
Bacillus malariae. Canine distemper, a sometimes deadly disease
in dogs that causes symptoms like fever and vomiting, was linked to a series of different
bacteria before it was finally proven to be a virus in the 1920s. And the familiar virus influenza, or the flu,
was misidentified as a bacterium in eighteen ninety-two, by a colleague of Koch’s. The bacterium came to be known as Haemophilus
influenzae. To study the flu, researchers needed samples
of spit and snot from people with obvious symptoms. But one thing that made influenza hard to
study was that, even though the flu usually reaches a peak in winter, the only time that
scientists could reliably find large numbers of flu-ridden folks at the same time was during
a pandemic. And those could be decades apart. So the first chance scientists had to check
the results from 1892 was during the next influenza pandemic… in 1918. Researchers were unable to replicate those
initial results. But it wasn’t clear at the time if it was
because of poorly controlled studies in the chaos of one of the worst pandemics in recent
history and the end of World War I, or if they were just… wrong. A vaccine was developed in New York based
on Haemophilus, just in case. There was at least one study around that time
that managed to find evidence of the right answer: influenza is a virus. It took until 1933 and another influenza pandemic
for scientists to prove without a doubt that the flu is caused by a virus, thanks to the
introduction of ferrets as a model organism. Ferrets were the only small mammals they could
find that actually get the flu and show symptoms similar to ours. So it seems like Koch’s Postulates, especially
the second, really hindered research into any disease that didn’t have a bacterium
behind it. Does that mean they’re useless? Not at all. Since the 1880s, scientists have tweaked Koch’s
postulates over time to match modern understandings of pathogens. Today, the focus isn’t just on microbes,
but on their genes. Using genetic sequencing, scientists can gather
information about all of the nucleic acids in a sample, whether DNA or RNA, and then
use a modified version of Koch’s postulates to figure out which genes are most associated
with disease symptoms. For example, in 1996 scientists at Stanford
came up with a new set of postulates with seven gene-centric points. By using gene sequencing, scientists can find
pathogens that haven’t been isolated and identified before. And there’s no need to culture them. Koch’s postulates provided a solid foundation
for researchers to begin linking diseases to their sources. Sure, there were a few mistakes, but they
provided a rigorous, testable basis for understanding disease. Even if we had to come along and make some
changes later. And even if some ferrets had to get the sniffles. Thanks for watching this episode of SciShow,
and thanks to our supporters on Patreon for making what we do possible. If you want to join them and help us, while
also getting some cool benefits, check out patreon.com/scishow. {♫Outro♫}

Here at SciShow, we talk a lot about the fascinating,
complicated, and often very weird stories of discovery and collaboration that led to
the science we know today. But one of the strangest is something we haven’t
covered in much detail before, and it’s a biggie: the decades it took to figure out
exactly what HIV and AIDS were, and how to prevent and treat them. Since the start of the AIDS crisis, some 70
million people have been infected with HIV, and 35 million of those people have died. Both those numbers are staggering in their
own way, and together, they tell the story of a disease that has led to an incredible
amount of loss, but also one that — if you’re lucky enough to have access to the right medicines
— is no longer a death sentence. So, in honor of World AIDS Day on December
1, we want to tell you that story. There’s a lot to cover, so we’ll do it
in two parts. This episode, we’ll go over how we figured
out what HIV is, when the infection morphs into AIDS, and where we think the virus came
from. Next time, we’ll look back to the earliest
treatments, the arrival of antiretroviral drugs, which were complete game-changers,
and go over the creative ways scientists are now thinking about prevention and possibly
even a cure. But first, the basics. HIV, or human immunodeficiency virus, is a
retrovirus that infects immune cells, most notably what are known as CD4 T cells. The “retrovirus” part just means that
the virus uses RNA — DNA’s more wily, less stable cousin — as its genetic material,
and that once HIV infects a cell, it makes a DNA version of its genome with a special
enzyme, then inserts that DNA into the host genome. If that sounds sneaky — well, it is. And it’s part of why HIV has been so difficult
to treat, which we’ll talk about more next time. Now, those CD4 T cells that HIV infects and
ultimately kills are a kind of white blood cell known as ‘helper’ T cells. When they recognize a threat, they pump out
proteins that help coordinate a bunch of different immune responses. You definitely want them around. HIV is spread by bodily fluids, including
blood, semen, vaginal fluid, and breast milk. That’s why HIV can be transmitted through
sex, dirty needles, breastfeeding, and any other swapping of fluids you might do — with
a major exception: saliva isn’t one of those fluids. Saliva is full of other stuff that prevents
HIV from being infectious, like antibodies and a bunch of antimicrobial proteins. So unless there’s a lot of blood in your
saliva for some reason, it can’t transmit HIV. When someone is first infected, they might
feel like they have a bout of the flu, with a fever, headache, rash, sore throat, and
muscle and joint pain. That’s because the virus is infecting lots
of cells and the immune system is trying to fight it off. But within a few weeks those symptoms pass
because by then the person has specific antibodies that can keep the virus from running totally
rampant. After that, they usually feel fine for a long
time — in many cases, a really long time, like several decades. Until, one day, they don’t, because the
virus has finally killed off too many T cells, leaving the body unable to properly defend
itself against pathogens — anything that might be dangerous or infectious. That’s when someone is said to have AIDS,
or acquired immune deficiency syndrome. Usually AIDS is diagnosed once the person’s
T cell count falls below 200 cells per microliter of blood, which is well below the normal 500-1500,
or if they develop what’s called an opportunistic infection. These are infections that anyone with a reasonably
strong immune system would be able to fight off, easy-peasy. But because HIV has obliterated most of their
T cells, AIDS patients get sick. And, they can die. Most of the time it’s an opportunistic infection
that killed them. So, some of that was probably familiar to
you, but pretend for a moment that you’ve never heard of HIV or anything else I just
mentioned. Because back in the ‘80s, we didn’t know
these basic facts. All doctors knew was that suddenly, healthy
young gay men were developing extremely rare infections and cancers — and, it was killing
them. One of the first people to notice the pattern
was an immunologist at UCLA. Between the fall of 1980 and the following
spring, he saw a string of five patients, all gay men in their 20s or 30s, with an unusual
kind of pneumonia. There was a fungus growing inside their lungs. Normally, the fungus was totally harmless
and would never infect the lungs, but in these men it had, and it was making it hard for
them to breathe. The patients also had oral thrush — basically
yeast infections in their mouths — and few CD4 T cells. By June, when the immunologist wrote up the
results for the CDC’s weekly Mortality and Morbidity report, two patients had died. A month later, a dermatologist in New York
chimed in with a similarly disturbing report, this time with Kaposi’s sarcoma, a rare
cancer where patients develop blotchy purple lesions on their skin. In two and a half years, 26 young gay men
in New York and LA had been diagnosed with Kaposi’s. Some also had the weird fungal pneumonia,
and 8 had died. It’s hard to imagine now, but at this point,
scientists had no idea what was making people sick. They didn’t know if it was some sort of
toxin or a pathogen. And if it was an infection of some kind, they
didn’t know how it was spreading. That meant they couldn’t warn people about
how to protect themselves. The association with gay men, though, was
certainly striking, and early on, many called the mystery disease GRID, for gay-related
immune deficiency. Lots of people would talk about it as the
“gay cancer” or “gay plague.” But the disease wasn’t limited to gay men. It was turning up in hemophiliacs — people
whose blood doesn’t clot properly and are treated with clotting factors taken from other
people’s blood. Doctors were also seeing cases in IV drug
users, women, infants, and heterosexual men. In particular, 20 recent immigrants from Haiti
had gotten sick, and none said they were gay. Those clues were important, because they told
scientists the disease — which had finally been given the name AIDS — was probably
infectious, and probably transmitted by blood. There were other diseases that spread in similar
ways, like hepatitis B. So in March of 1983, the CDC issued a warning
that doctors needed to be careful about blood transfusions, and that the disease seemed
to spread through both gay and straight sex. Debates about the specifics, including whether
it could spread through saliva, would happen later. But what was the infectious agent? The race was on for scientists to figure out
what was causing the disease. French molecular biologist Luc Montagnier
suspected a virus because at the time, the blood products hemophiliacs used were filtered
for things like bacteria and fungi. But viruses were too small to catch. So along with his colleague Françoise Barré-Sinoussi,
he searched cells taken from AIDS patients and found a retrovirus. Around the same time, Robert Gallo at the
NIH in the US also identified a retrovirus in samples from AIDS patients. Both groups published their work in May 1983,
and shortly afterward another team found yet another retrovirus. All the viruses had been given different names,
and at first, it’s wasn’t totally obvious that they were the same thing. But they were, and in 1986, the cause of AIDS
had been given an official name: HIV. So, HIV was the problem, but where had it
come from, and why had the epidemic struck now, in the decade of big hair and Michael
Jackson? While some researchers were scrambling to
identify whatever it was that made AIDS infectious, others noticed that macaque monkeys also seemed
to suffer from an AIDS-like disease. One group decided to take some blood samples
from these sick monkeys, and in 1985 they found a virus that was similar to HIV. It was eventually called SIV, for simian immunodeficiency
virus. Researchers started to think that HIV might
have come from our primate relatives, jumping the species barrier. After a lot of work, they figured out that
the virus behind the epidemic was very similar to the chimpanzee version of SIV, and they
were the ones who had passed it to us. But how exactly? There’s no real way to put this delicately,
but most scientists agree that the reason why SIV made the leap into humans — what’s
called a spillover — is because we had a taste for bushmeat, or wild game. In this case, monkeys and chimps. This is known as the cut-hunter hypothesis. In the course of butchering a chimpanzee,
some SIV-infected chimp blood enters a small cut on the hunter’s hand. Or, a bit of blood splatters in their mouth. The virus is close enough to human biology
to infect the hunter, and over time, if the hunter passes the virus along to enough people,
it evolves into the HIV we know today. Spillovers like these happened many times
— we can tell because the virus mutates quickly, and by looking at genetic differences,
we can identify multiple lineages of the virus, each one corresponding to a spillover. We’ve traced the current epidemic to just
one of these, called ‘M’ for main. By analyzing chimpanzee pee and poop, researchers
think the chimps who passed that version of the virus to us lived in southwestern Cameroon,
in the forests near the Congo. And based on the oldest blood samples we can
find that we now know have HIV in them, which are from 1959 and 1960, scientists estimate
that HIV-1 first infected humans around 1908. If that seems like a long time ago, well,
it takes a while for a virus to take off. By the 1920s, it’s thought that the virus
traveled downriver — in a person, of course — to the burgeoning city of Kinshasa, then
known as the Belgian colonial city of Leopoldville. There weren’t many women around other than
prostitutes, so experts think HIV spread that way, and possibly through injectable drugs
the colonists used to treat some tropical and venereal diseases. This was before disposable syringes, and nurses
were trying to treat lots of people with just a few of them, so the syringes may have only
been rinsed with alcohol before being used on the next patient. So the very methods meant to stop the spread
of disease may have actually been
encouraging it. With time, infected people in Kinshasa left
to go to other places, and they did the unavoidable: they brought the virus with them. Because the virus mutates so quickly, we can
group the viruses into 9 different subtypes and get a sense of how HIV traveled around
the world from Central Africa. Several subtypes spread to other parts of
Africa. Subtype C went south and then landed in India. Subtype B went to Haiti — and then, through
several quirks of history, came to the US. First, in 1960, when the Belgians left the
Congo, French-speaking Haitians started to arrive in the Congo to work as doctors, lawyers,
and other professionals. But with the creation of Zaire in 1965, the
immigrants felt unwelcome, so they went back to Haiti, bringing HIV with them. There, HIV expanded especially quickly, possibly
because of a plasmapheresis center where people could get paid to donate their blood plasma. The center used a machine that mixed the blood
of different donors, allowing viruses to transfer. By 1982, nearly 8 percent of a group of young
mothers in a Port-au-Prince slum were HIV-positive — an astoundingly high number. HIV is thought to have entered the US around
1969, with just one infected person or unit of plasma from Haiti. It took about a decade for anyone to notice,
but by then it was too late. The epidemic had begun, and HIV was not only
in the Americas, but Europe and Asia, too. And now that it was here, we needed to figure
out how to fight it. But we’ll get to that in the next episode
of this mini-series. In the meantime, thanks for watching this
episode of SciShow, and if you want to learn more about HIV and all kinds of other science,
you can go to youtube.com/scishow and subscribe.

SciShow is supported by Brilliant.org. [♪ Intro ] Some animals are way smarter
than we give them credit for. Crows can invent tools, some spiders customize
hunting techniques, animals have even been observed medicating themselves to treat illnesses. But animal behavior isn’t always what it
seems, and this self-medication is a great example of that. There’s actually a whole field about this
subject, called zoopharmocognosy, and it tends to pop up on the internet
from time to time. For example, you might have read how elephants
eat a certain tree to induce labor. Or that some primates eat specific plants
to get rid of parasites. But as cool as that sounds, and it sounds
pretty cool, some of those stories are a bit problematic,
at least scientifically. In some cases, the research isn’t nearly as
solidified as a lot of articles will make you believe. So here are six examples of zoopharmacognosy
and what the research really says. Although they are not the most famous examples,
the best-studied cases of zoopharmacognosy are actually in insects, like tiger moth caterpillars. These insects eat multiple species of plant,
but some of them are a bit unusual, because they contain harmful chemicals called pyrrolizidine alkaloids, or PAs. These chemicals reduce the caterpillars’ ability to grow, but there’s also a pretty big benefit to eating them: PAs protect the
caterpillars against parasitoids. And a small caterpillar is better than a dead
caterpillar any day. These caterpillars are parasitized by several
species of insect, including some flies that can make their lives
pretty horrible. The flies lay their eggs on the caterpillars,
and when they hatch, the young maggots burrow into the caterpillars and begin eating them alive. But if a caterpillar’s tissues are laced
with PAs, it has a chance to survive this horror, because the alkaloids are even more
toxic to the maggots than they are to the caterpillars. In a paper published in PLOS One in 2009,
researchers validated that idea in the lab, and they even found that parasitized insects
ate more alkaloid-laced food than their unaffected counterparts. Kind of like they were taking more medicine. It’s unclear exactly how much they know
why they’re doing what they’re doing, and the results were slightly different depending
on how many fly eggs a caterpillar had on it. But one way or another, it shows that they’ve
found a treatment to kill the flies that ail them. It’s not just caterpillars that do this,
either. Another insect that uses medicine to combat
body-snatching parasites is our old friend the fruit fly. If you’ve ever forgotten a peach in the
back of your pantry, you probably know that these flies are attracted to rotting fruit. They lay their eggs on it so that, when they
hatch, the little maggots have a sweet meal right in front of them. But sometimes, old fruit has yeast growing
on it. And as the yeast cells break down sugars in
the fruit, they make ethanol, a type of alcohol that gives those
baby flies a boozy meal. Ethanol isn’t good for developing baby anythings,
but fruit flies can tolerate some of it because they have an enzyme to break it down. Still, generally, female flies do prefer to
lay their eggs on fruit with low levels of ethanol, except when parasitoid wasps are
around. Kind of like with the caterpillars, tiny wasps
can lay their eggs in fruit fly maggots, and eventually, the wasp larvae
will devour them alive. But the wasps aren’t as tolerant of ethanol
as fruit flies. For them, it causes various organ defects,
and research published in 2012 showed that wasps were more than twice as likely to die if they parasitized flies that had been consuming ethanol. What’s especially cool is that another study,
published a year later, showed that female fruit flies decide whether or not to lay their eggs in boozy fruit based on the risk of parasitism. In the experiment, female flies that saw female
parasitoid wasps preferred to lay their eggs in high ethanol food sources. But flies who were shown male wasps, who don’t
lay eggs and so don’t pose a parasitism threat, preferred low-ethanol fruit. Like with the caterpillars, though, this doesn’t
necessarily mean the flies learned that ethanol was medicine. The researchers suggested that, instead, seeing
a female wasp might trigger changes in the fly’s brains that cause them to prefer it. Although these insect stories are great, the
whole idea of zoopharmacognosy really gained popularity based on work by primatologists. Over the years, they observed various monkeys and apes eating plants used by local humans to treat ailments, especially intestinal parasites. This led them to hypothesize that the animals
were also using plants as medicine, and their ideas trickled down into
pop culture from there. But the truth is, in a lot of these cases,
there just isn’t a ton of evidence, because these hypotheses are much harder to test in
primates compared to with insects. For example, it’s not really ethical, or
practical, to put a bunch of monkeys in lab, and then give some of them parasites and see what
they choose to eat. So scientists mostly have to rely on circumstantial evidence they gather by basically stalking primates in the wild. But those studies have been really interesting. One example was from a paper published in
2001, where researchers recorded an odd behavior in chimpanzees in Tanzania. First thing in the morning, on an empty stomach,
the chimps would fold up a leaf, often from an Aspilia plant, and then swallow it whole,
without chewing. Other researchers had seen similar things
before, but in this paper, the scientists took their work further. They recorded 14 instances of this behavior
and then followed the chimps closely to see, like, how everything came out. They were only able to observe pooping in
seven of the animals, but for those seven, they found that the leaves passed through
the chimps’ guts pretty much intact. More importantly, they noticed that there
were often adult nematode worms present in the poop, parasites that spend part of their
life cycle in the chimps’ intestinal walls. The researchers didn’t find evidence of
any nematode-killing chemical in the Aspilia leaves, though, like you might guess. Instead, they think the leaves may have more
of a mechanical action. They have rough, slightly bristly surfaces,
and the scientists think that allows them to physically scrape the worms off the chimps’
intestinal walls. Kind of like swallowing a scrub pad. As you can imagine, the leaves also irritate
the stomach, which makes it secret more gastric acid. Then, the acid passes through the intestine
as well and may further repel the worms. Of course, the sample size here is pretty
small, and the researchers couldn’t experimentally test whether the leaves actually dislodge any parasites. So before we say anything for sure, we’ve got to get some science way more up close and personal with those chimp intestines. All examples of zoopharmacognosy aren’t
about parasites, though. Some animals self-medicate for other reasons. For example, red colobus monkeys living on the island of Zanzibar may use charcoal to prevent upset tummies. Farmers in Zanzibar have planted two species
of non-native trees, mango and Indian almond, that have protein-rich, nutritious leaves
that also happen to be loaded with tannic acid. Tannic acid binds to proteins during digestion,
which makes food less nutritious and also causes symptoms like nausea and vomiting in
humans and, presumably, in monkeys. In high enough doses, it can also be toxic
to liver cells. So to eat the mango and almond leaves safely,
the colobus monkeys appear to take advantage of another resource that humans have inadvertently
provided, charcoal. Local farmers burn wood in outdoor kilns to
make charcoal for cooking fuel. And colobus monkeys visit these kilns when
they’re not in use to eat the bits of charcoal left behind. Charcoal doesn’t have any nutritional value,
but it is good at absorbing things. That’s why we use activated charcoal to
treat people who have ingested certain types of poison. In 1997, when researchers tested the samples
of charcoal the monkeys were eating, they found that they weren’t as good at absorbing
tannic acid as medical-grade activated charcoal, but they were surprisingly effective. That made them hypothesize that eating charcoal
allows the monkeys to safely eat the nutritious almond and mango leaves. This may even be a learned behavior, too. Colobus monkeys that don’t live near farms and don’t eat these leaves haven’t been observed eating charcoal. And when researchers left some out, the animals
had no interest in it. To get really convincing evidence that the
monkeys are using charcoal as medicine, though, you would have to do actual experiments, like
feeding the monkeys almond leaves without charcoal and seeing if they got sick. But that’s logistically pretty challenging,
and also just kind of mean. If you’ve tried doing the monkey bars on
the playground recently, you might have found that as you’ve gotten older you’re a little
less good at that and your arms got pretty sore. And you might have even later treated that
with a pain-killing rub like Icy Hot. If you did, you might not be alone. Based on some evidence, orangutans might do
something similar after a long day swinging through the trees. Starting back in 2003, scientists studying orangutans
in Borneo noticed some of the animals chewing up the leaves of the Dracaena plant, spitting them out, and massaging the spit-leaf mixture
on their arms and legs. The orangutans never swallow the Dracaena
leaves, and they don’t rub any other leaves on their body like this, so scientists got curious. They learned that local people used Dracaena to treat sore muscles, and after some chemical analyses, they found that there was good reason
for that: The plants contain chemicals called saponins, which can have anti-inflammatory properties. Specifically, they inhibit the production
of inflammatory cytokines, signaling chemicals that promote redness and swelling. Muscle soreness after hard exercise is caused
in part due to this inflammation. So it’s possible that the orangutans were using the chewed up Dracaena leaves as a pain-killing rub. What makes this more likely is that most of
the animals observed doing this were females who were hauling the extra weight of their
offspring around and might have had some extra sore arms. But so far, only ten orangutans have been
observed using Dracaena, and researchers can’t exactly ask them
how their arms feel. For all we know, the leaf-spit mixture just
makes their hair really soft and shiny. They’re instagram influencers. Finally, one example of zoopharmocognosy that
has gotten a lot of attention is the elephant and the red seringa tree. As the story goes, a researcher studying elephants
in Kenya observed one very pregnant elephant walk many kilometers out of its way to devour
this tree. They had never seen any of their elephants
eat this plant before, so it seemed odd that the pregnant one made such an effort to do it. Then, four days later, the elephant gave birth. When the researcher talked to local women
about this, they told her that sometimes they used a tea made from seringa leaves to induce uterine contractions and labor. So the researcher hypothesized that, maybe,
the elephant was using the plant the same way. But even though popular literature cites this
example a lot, it’s really not conclusive. For one, it’s not clear which chemical in
the seringa is responsible for inducing uterine contractions in humans. Or, if it has the same effect in elephants. Maybe that elephant would have given birth
in four days no matter what she ate. Generally speaking, we also don’t know how
often pregnant elephants eat this tree. At the moment there’s just this one recorded
observation and a cool hypothesis that needs more testing. All these examples go to show that zoopharmacognosy
is really a very cool field, and that, in some cases,
there is very strong evidence for it. But in other cases the jury is still out. There’s still a lot scientists need to learn,
and there are research methods they need to develop. But one way or another, this all raises interesting
questions about animal learning, and whether we can discover potential medicines for ourselves by watching how animals deal with their ailments. We just probably shouldn’t come to those
conclusions too fast. Which is true of anything. We have to apply appropriate methodology and
logic to any new discovery. And if you want to work out your analytical
thinking muscles, check out the Logic course on Brilliant.org. You’ll get to pretend you’re a 21st century
Sherlock Holmes when you learn ways to predict the outcome of a competition or unlock how to tell if a statement is true or false. And you’ll be learning multi-level thinking
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So, you know in Game of Thrones, there’s
this character—smells really bad, they call him “Reek”? Turns out, that could actually be caused by medical conditions that we know of, medical conditions that cause you to emit odors that go way beyond the typical stinky armpit. In some cases, you might reek of boiled cabbage,
or sweaty feet, or even rotting fish. These conditions are rare,
but their symptoms can be pungent, and sometimes also downright dangerous. Unusual body odors are often a sign of a bigger
problem—specifically, a defect in the way your body is breaking down, or metabolizing, your food. For example, there’s the condition known
as trimethylaminuria— also known as “fish odor syndrome”. Patients with this condition are said to smell
like decomposing fish, because their bodies don’t break down a compound called trimethylamine,
which emits the je ne sais quoi of fishiness. Now, everyone’s body produces trimethylamine—specifically, in the gut, where bacteria excrete it while helping us digest foods like eggs, liver, and fish. Normally, having all that trimethylamine
in your body is not a problem, because it’s converted into an odorless molecule,
thanks to a special enzyme in the liver, known as a flavin-containing monooxygenase. But people with fish odor syndrome can’t
metabolize the smelly compound, because they have mutations in the gene that produces that enzyme. Without enough of that working enzyme, the
trimethylamine builds up, and has nowhere to go but out with your bodily fluids—in
your sweat, urine, even on your breath. But people with the condition do have some options. They can change their diets so there are fewer
of the precursor chemicals that get broken down into trimethylamine. It’s one of the only times your doctor
will actually tell you not to eat your broccoli, or your brussels sprouts! Infusions of antibiotics can also help wipe out some of the bacteria that are making the trimethylamine. These rarely solve the problem entirely, but
the good news is that apart from the smell, there isn’t any major health problem associated
with fish odor syndrome. Which is not the case for a disorder that gives people the distinctive whiff of sweaty feet. This condition, known as isovaleric acidemia,
can cause brain damage, and even death, particularly in young children. Here, patients have a genetic mutation that
leads to a deficiency in an enzyme called isovaleric co-enzyme A dehydrogenase. This enzyme is important because it helps
break down the amino acid leucine. Without this enzyme, leucine can only be broken
down part-way. And the compound that’s left over from this
process, an acid called isovaleric acid, starts to build up. Isovaleric acid smells kind of like cheese,
and it’s the same chemical that makes your sweaty feet smell. The bacteria hiding out between
your toes produce this acid when they’re chomping away on leucine. But while isovaleric acid isn’t exactly
pleasant to smell outside your body, it can be downright damaging to the inside. It’s not exactly clear why, but a build-up
of isovaleric acid tends to have the most dramatic effects on the central nervous system. In large amounts, it’s toxic to neurons, which can result in developmental delays in many patients. And because this enzyme deficiency makes it
difficult to digest breast milk or formula, dangerous symptoms can start
appearing very soon after birth. In severe cases, infants just a few days old
will refuse to eat and begin to have seizures. There is, so far, no cure for isovaleric acidemia,
but some treatments— like avoiding foods rich in leucine, and taking supplements of other, non-threatening amino acids— can help keep patients safe. Finally, peculiar symptoms and even stranger
smells can result from another, similar disorder known as hypermethioninemia. In this case, the problem is having too much
of a different amino acid: methionine. Methionine is the rare amino acid that contains
sulfur, an element known for its pungent odor. And when methionine isn’t metabolized properly
in your body, it can result in large amounts of dimethylsulfide, which produces a smell
similar to boiled cabbage. Sometimes the condition comes about just because
you’ve eaten too much methionine, which is in protein-rich foods, like meat and cheese. But if the cause is genetic, it can be due
to mutations in one of several genes that are responsible for making the enzymes that help break down methionine. Without those enzymes, patients sometimes have that cabbagey smell in their sweat, breath, or urine. And strangely, not everyone with the disease
has symptoms—in fact, most people don’t. But in some, it can be serious. In severe cases, the inability to process
methionine can lead to neurological problems and muscle weakness, among other problems
in the nervous system. Again, treatment usually involves avoiding
foods that contain methionine, as well as taking supplements to make sure that the body
is getting what it needs. So, run-of-the-mill BO is nothing compared
to the very real medical conditions that can create unpleasant smells. There are a lot of things that can go wrong
when your body metabolizes food, and weird odors are just one way
to help spot and diagnose them. This episode of SciShow is brought to you
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see which regions around the world their ancestors came from, and learn how their DNA influences
facial features, hair, sense of taste and smell, sleep quality and more. You can also connect with people who share
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to learn about my health, ancestry, and personal traits through my DNA. I’ll also learn about my genetics related to
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It almost sounds like a Sherlock Holmes case: A 61-year-old man staggers into a Texas emergency
room feeling light-headed, nauseous, and dizzy. The nurses think he looks kinda hammered,
so they give him a Breathalyzer test, and sure enough, his blood alcohol concentration
clocks in at a very drunk .37 percent. But thing is, the guy claims he hasn’t had
a single drink today. In fact, he says he’s been experiencing
sudden and unexplained bouts of drunkenness for years. So what’s up? Is the guy a closet drinker?
Is he suffering some kind of amnesia, or sleep-boozing, or what? The doctors decide to check the man’s pockets
for hidden booze, then monitor him in an isolated hospital room for 24 hours. They have him
eat a lot of carb-heavy foods while staff take various readings and watch what happens
to his blood alcohol content. What they eventually find, is that the guy
has an over-abundance of brewer’s yeast in his digestive system, and it’s basically
turning his guts into a fermentation vat, converting carbohydrate sugars into ethanol,
and getting him sloshed. As you’ve probably guessed by now, this
story actually happened, back in 2010. And in the end, the man’s doctors diagnosed
him with auto-brewery, or gut fermentation syndrome. Basically, his digestive system
was turning carbohydrates into alcohol. Cue the beer belly jokes.… Here’s what his doctors figured was happening: When most people eat yeasty foods, the yeast
passes right on through their body. But sometimes it’s possible for that yeast to stick around
in larger numbers. The Texan man’s troubles seem to have started
after he completed a hardcore round of antibiotics that wiped out his good gut bacteria, eliminating
the competition and allowing yeasts and other fungi to take over. So whenever he’d eat carbohydrates, the extra
yeast in his digestive system would start fermenting those carbs into alcohol, which
would end up in his bloodstream. He was literally getting drunk on bread. The doctors treated the man by having him
take antifungal drugs and probiotics to restore his good bacteria. They also had him eat a
low-carb diet help to keep the yeast in check. Now, this wasn’t the first-ever case of auto-brewery
syndrome. Some children with short bowel syndrome — an
intestinal condition that makes proper nutrient absorption difficult — have also shown signs
of extra yeast causing intoxication. And researchers in Japan have documented similar
reports of serious digestive yeast infections and spontaneous tipsiness, dating back to
the 1970s. Even so, this syndrome is both rare and controversial,
because all we have is this handful of mysterious case studies. It’s just hard to figure out what’s actually
causing the problem without more research — like a controlled clinical trial. Plus, when it comes to getting drunk without
drinking, an over-abundance of yeast may not be the only factor involved. There’s also a problem with certain enzymes. Normally, alcohol gets broken down by particular
liver enzymes. But in some people, genetic mutations mean
they don’t produce those enzymes properly. So they can end up feeling drunk after drinking
a relatively small amount of alcohol. This mutation affects a disproportionate number
of Asian people — about one in three, which could help explain why Japan has the highest
number of reported gut fermentation syndrome cases. Combine extra yeast with a rice-heavy diet
and abnormal enzymes and you might find yourself getting accidentally sauced as those carbohydrates
turn to ethanol that doesn’t get processed quickly enough. It’s pretty easy to test for these enzyme
deficiencies, but so far there’s no definitive test for auto-brewery syndrome in people with
the usual enzymes. Since it’s so difficult to clearly diagnose,
it would be hard for researchers to set up studies and trials. So, until there’s a better way to diagnose
it, auto-brewery syndrome is a condition that will probably continue to be rare and mysterious. Thanks for watching this episode of SciShow,
which was brought to you by our patrons on Patreon. If you want to help support this
show, just go to patreon.com/scishow. And don’t forget to go to youtube.com/scishow
and subscribe!

A sore throat can be a sign of all kinds of
medical maladies. You might have caught a cold from your coworkers,
or just cheered too loudly at the big game last night. But if it feels like there’s an irritating
lump in your throat, there might actually be something stuck back there: a whitish-yellowish
tonsil stone. These hard globs come from the food bits,
dead cells, and other junk in your mouth. But even though they might be a little weird
and uncomfortable and gross, they’re not really dangerous. Your tonsils are part of your lymphatic system. They work with a bunch of other tissues to
get rid of waste, and fight off infections. There are actually three different groups
of tonsils, but tonsil stones mostly show up in the palatine tonsils The palatine tonsils are those two squishy
patches at the back of your throat that you can see in the mirror if you open your mouth
wide enough. The palatine tonsils are full of tonsillar
crypts, which are deep folds of tissue that are designed to lure in bacteria and maximize
the amount of tissue that those bacteria touch. That way, lots of immune cells can be exposed
to potential pathogens, and start to build up a targeted immune response with antibodies
to fight them off. Unfortunately, when you have cozy crevices
for bacteria, sometimes they get a little too comfortable. These crypts can collect dead cells, extra
mucus, and food debris or other particles that somehow end up in your mouth – which
provide a delicious breeding ground for lots of different microbes. After a film of bacteria forms, these goopy
lumps can start to calcify, becoming hard structures made of calcium and other minerals. The solid lumps that form are called tonsil
stones, or tonsilloliths. Tonsil stones can vary in size from a couple
millimeters to a couple centimeters. Sometimes people just swallow them, or sometimes
they stick around and can irritate your throat. Some bacteria that have been found on tonsil
stones produce lots of sulfur compounds, which might cause bad breath. But that’s usually the worst of it. It’s really rare for tonsil stones to get
big enough to be dangerous and make swallowing painful or difficult. If you want to get rid of them, you can try
to pop them out using a brush or some gargling. Or you can go to an ear, nose, and throat
doctor for extra help. Tonsil-removing surgery is a last resort,
if these chunks form all the time, or become severely irritating. Other than surgery, there’s not much you
can do to stop tonsil stones from forming. They’re just one of those weird things your
body does sometimes. But at least they’re not dangerous. Thanks for asking, and thanks especially to
all of our patrons on Patreon who keep these answers coming. If you’d like to support us on Patreon,
you can go to patreon.com/scishow. And don’t forget to go to youtube.com/scishow
and subscribe!

My friend the toadstool, he just left the
party, ‘cause there wasn’t mushroom! And it’s too bad, ‘cause he was a real
fun-guy. Ok…ahh… in addition to being fun guys, fungi
are incredible organisms. They make up their own kingdom in the eukaryotic
domain of the tree of life, separate from animals and plants. This kingdom includes everything from microscopic
organisms like yeast and mold, to those familiar dome-shaped mushrooms you can find at the
grocery store… or in Super Mario. And since there are so many different kinds of
fungi, it’s no wonder that some of them have pretty crazy talents. [Music Playing] First, we have a classic fungus: the mushroom.
The magic mushroom, to be precise. These mushrooms contain the chemical compounds
psilocybin and psilocin In the human body, the psilocybin gets broken
down into psilocin, which is the active form of the hallucinogenic drug. The chemical structure of psilocin is similar
to the neurotransmitter serotonin, which normally sends signals between brain cells to regulate
things like mood, memory, and sleep. So, psilocin tricks the brain into activating
those serotonin receptors. And this can cause hallucinogenic effects,
like changing thought patterns and mood, visual distortions, and even a sense of euphoria. There’s some sketchy anthropological evidence
that magic mushrooms could have been used in religious ceremonies by different cultures, but those theories are controversial among historians. The mushrooms hit the U.S. cultural scene
in the 1950s, though, after a mycologist, a scientist who studies mushrooms, brought
the practice back after a trip to Mexico. By the 1970s, these mushrooms were illegal
in the US, after being widely used as a recreational drug. But they may be making a comeback for another
purpose: psychotherapy. With permission from the U.S. government,
certain researchers are carefully conducting studies to explore the benefits of small doses
of psilocybin to treat conditions like post-traumatic stress disorder and chronic depression. Some mind-altering fungi have more dangerous
side effects. In fact, one of the most famously horrifying
events in early American history may have a fungal infection to blame. Ergot fungi are members of the genus
Claviceps. And the most well-known variety is Claviceps
purpurea, which grows on rye and other grains. The fungus produces some toxic nitrogen-containing
compounds called alkaloids. In particular, it creates lysergic acid.
Which might sound familiar because it’s used to synthesize the psychedelic drug lysergic
acid diethylamide, better known as LSD. Lysergic acid alone can lead to mania and
psychosis, while other alkaloids in ergot fungus can cause seizures and spasms, headaches,
nausea, crawling skin, and vomiting. As it turns out, many of these fun symptoms are very similar to the effects of the so-called “bewitchment” recorded in the Salem Witch
Trials in 1692, where both women and men were accused of witchcraft, tried in court,
and even executed. At the time, rye was a staple in the diets
of Salem residents. And warm, humid weather the previous year
would have made a prime breeding ground for ergot fungus. Ergot poisoning probably can’t account for
all of the hysteria surrounding the witch trials, but it all could have started with
some fungus in their food. Pop culture is full of zombies, but it’s
a relief to know that the apocalypse is not upon us… yet. The same can not be said for camponotini
ants, who face a unique threat to their colonies: zombie ants! A particular type of fungus called Ophiocordyceps
unilateralis can take control of the ants it infects. The infected ants show extremely specific behavior, they travel down to a lower level in the forest where the air is just humid and cool
enough, and find a leaf on the north side of a plant about 25 centimeters above the
ground. Then, they clamp down onto the underside of
the leaf and die. After a few days in these ideal conditions,
thin stalks of fungus sprout from the ant’s head so that spores can be released, in the hope of infecting more ants and continuing the cycle. Scientists aren’t sure yet how this fungus
can so carefully control the ant’s behavior, but this isn’t the only parasite to have
evolved mind-controlling abilities. One of the great medical achievements of the 20th century was the discovery and isolation of the antibiotic penicillin. Without a reliable way to kill off the bacteria
causing an infection, something a simple as a scratch could turn out deadly. But, in the late 1920s, bacteriologist
Alexander Fleming, noticed that Penicillium notatum mold had contaminated one of his petri dishes and killed all of the bacteria it touched. That was because the Penicillium mold produced
a bacteria-killing chemical that Fleming eventually called penicillin. It attacks the enzymes that build the bacterial
cell walls, so the walls fall apart, and the bacterium dies. Researchers at Oxford University then worked
on mass-producing, purifying, and testing the antibiotic, which went on to save thousands
of soldiers from death by infection in World War II. Pretty incredible stuff for a bread mold! And, penicillium isn’t the only life-saving
fungus out there. Tolypocladium inflatum seems pretty boring at first glance. It lives in Norwegian soil and can infect
beetle larvae. But this fungus produces a compound called cyclosporin, which is really good at suppressing our immune systems. It sounds dangerous and bad when you put it that way, but cyclosporin is an important drug that keeps organ implants from being
rejected. Normally, the patient’s immune system would
see the implanted organ as an intruder and attack it using the body’s first line of
defense: the T-cells. But cyclosporin inhibits those cells, preventing
the attack, and protecting the new organ as the patient’s body adjusts. And continued low doses of this drug can keep
organ transplant recipients healthy for years. When you think fungi, you usually think…like, pretty small. Like, cute-little-mushrooms-in-the-forest small.
Or even microscopic-mold small. But it turns out that some fungi can get huge. In fact, the largest living organism on the
planet is a massive honey fungus, of the Armillaria solidipes variety. This honey fungus has genetically identical
cells that can communicate and coordinate with each other, which, by one biological
definition, makes it a single organism. It’s estimated to cover around 9.6 square
kilometers in Oregon, and may be thousands of years old. But it’s not obvious how big this thing is. Clumps of mushrooms will appear above the surface
of the soil to release spores, but most of the fungus exists underground. Root-like rhizomorphs search for new host
trees to infect, while a network of thin, tube-like filaments called mycelia absorb
nutrients from the soil to keep this fungus growing. Not many people notice Pilobolus
fungus, since it’s a couple centimeters tall and mostly grows on… manure. But this unglamorous fungus has a secret superpower. During its reproductive phase, it forms thin,
pale stalks, called sporangiophores, with bulbs at the end containing spores, called
the sporangium. Pressure builds in the bulb until it eventually
bursts, sending the spores shooting around two meters away into nearby grass, so cows can eat it and the circle of life can continue. Now, that might not sound very impressive,
but these spores are accelerated at around 20,000 g’s. To put it in perspective, the shot coming out of a shotgun probably maxed out at around 15,000 g’s. That is a lot of acceleration for a tiny fungus. Death Cap and Destroying Angel mushrooms are
easily mistaken for edible fungi. But, as you might’ve guessed from their
names, they contain some of the most deadly substances known to humans. Other dangerous fungi include the deadly webcap
and the fool’s webcap. Both webcaps are part of the Cortinarius
genus and look like common brown mushrooms that you can eat. But, they produce a toxin called orellanine, which can cause kidney failure, and sometimes death. Plus, it can take anywhere from two days to
three weeks for symptoms to show up, so poisoning can be really hard to diagnose. The Japanese fungus Podostroma cornu-damae has some particularly nasty effects as well. Eating this rare red fungus causes altered
perception, severe upset stomach, hair loss, peeling skin, and even shrinking of the cerebellum, the part of your brain responsible for movement and coordination. The fungus is so rare that not many cases
of poisoning have been reported, but most of the known cases have been fatal. So it’s probably not a great idea to go
around eating random wild mushrooms. To make cheese, milk has to be soured, causing the solids, or, the curds, to separate from the liquids, or, the whey. The curds are then mixed with some other stuff, before they’re processed into the final cheese product. In the case of some popular cheeses like Roquefort, a type of blue cheese, this includes deliberately contaminating the curds with
fungus! Penicillium roqueforti is another
bread mold, from the same Penicillium genus as the life-saving antibiotic. The mold produces enzymes that break down
proteins in the cheese curds, helping create a distinctive smooth texture and strong, tangy
taste. Legend has it that people would place loaves
of bread in the caves surrounding the Roquefort region of France, hence the name. The loaves would grow moldy and dry out, be
pulverized into a powder, and then added to the cheese, giving it that delightful blue
veiny appearance. Nowadays, Penicillium roqueforti can be purchased
in stores, so you can make your own fungus-filled blue cheese at home! Humans have been consuming alcoholic beverages
for at least 7,000 years. And it turns out making beer wouldn’t be
possible without the help of a fungal friend named yeast. Specifically, a yeast called Saccharomyces cerevisiae. See, in beer brewing, grains are cooked in
water to form a mash. And then, they’re boiled to break all the starches down into simpler
sugars, and flavoring agents like hops are added. Once this mixture cools down, the yeast is
added, and that’s when the magic happens: Yeast eat all those sugars in the mash to
give them energy to reproduce, in a chemical process called fermentation. And they also generate a lot of waste, in
this case, carbon dioxide and ethanol. The carbon dioxide is what gives the beer
its characteristic fizz, while the ethanol is what gives humans their characteristic buzz. Thank you for watching this episode of SciShow,
which was brought to you by our patrons on Patreon. If you want to help support this
show, you can go to patreon.com/scishow. There’s a bunch of cool stuff that you can get there. And don’t forget to go to youtube.com/scishow
and subscribe!